Neurodevelopmental disorders are characterized by deficits in communication, cognition, attention, social behavior and/or motor control. Previous studies have pointed to the involvement of genes that regulate synaptic structure and function in the pathogenesis of these disorders. One such gene, GRM7, encodes the metabotropic glutamate receptor 7 (mGlu₇), a G protein‐coupled receptor that regulates presynaptic neurotransmitter release. Mutations and polymorphisms in GRM7 have been associated with neurodevelopmental disorders in clinical populations; however, limited preclinical studies have evaluated mGlu₇ in the context of this specific disease class. Here, we show that the absence of mGlu₇ in mice is sufficient to alter phenotypes within the domains of social behavior, associative learning, motor function, epilepsy and sleep. Moreover, Grm7 knockout mice exhibit an attenuated response to amphetamine. These findings provide rationale for further investigation of mGlu₇ as a potential therapeutic target for neurodevelopmental disorders such as idiopathic autism, attention deficit hyperactivity disorder and Rett syndrome.

中文翻译：

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mGlu7基因敲除小鼠的表型分析揭示了神经发育障碍的新含义。

神经发育障碍的特征在于沟通，认知，注意力，社交行为和/或运动控制不足。先前的研究已经指出了调节突触结构和功能的基因参与这些疾病的发病机理。其中一个基因GRM7编码代谢型谷氨酸受体7（mGlu ₇），这是一种G蛋白偶联受体，调节突触前神经递质的释放。GRM7中的突变和多态性已与临床人群的神经发育障碍相关。然而，有限的临床前研究已经在这种特定疾病类别的背景下评估了mGlu ₇。在这里，我们表明不存在mGlu ₇小鼠体内的表型足以改变社交行为，联想学习，运动功能，癫痫和睡眠等领域的表型。此外，Grm7基因敲除小鼠表现出对苯丙胺的减弱的反应。这些发现为进一步研究mGlu ₇作为神经发育障碍（如特发性自闭症，注意力不足过动症和Rett综合征）的潜在治疗靶点提供了理论依据。